Attacks sheep, goat, ox, horse, stag; and, experimentally, dog.
Causes: consumption of lupins, at a given stage of ripeness, from a
given part of a field, or from centre of a stack. Lupinotoxine,
conicine, methyl conicine, lupinine. Cryptogamic or bacterial poison.
Weak subjects, sheep and even ewes and lambs, suffer most. Symptoms:
Acute form: anorexia, fever, excited pulse and breathing, stupor, or
hyperæsthesia, vertigo, swellings on head. Poisonous lupins are first
rejected. Bloody nasal froth. In two or three days icterus. Urine may
be bloody. Fæces at first hard, coated, bloody, later dark brown and
often liquid. Emaciation. Death in 1 to 5 days. Chronic form,
gastro-enteritis, emaciation, anæmia. Nasal catarrh. Facial swellings
and sores. Lesions: hepatitis, nephritis, muco-enteritis, enlarged
spleen, icterus, blood extravasations; hepatic tissue, infiltrated,
cloudy, granular, fatty, later cirrhosis. Kidneys contain casts:
Spleen tumid, blood gorged. Prognosis: grave: acute cases die, chronic
may recover. Prevention: feed no lupins, avoid dangerous fields, wash
off poison from lupins with a soda solution. Ensilage with acid
producing fodder in alternate layers. Treatment: avoid alkalies, give
acids, purgative, castor oil, water. In horse, causes anorexia,
anæsthesia, dullness, stupor, colic, constipation, urinary irritation,
fever, slight jaundice, vertigo, orange nasal discharge, sores on
tongue and face, and lower part of limbs. Diagnosis. Prognosis
hopeful. Treatment as in sheep. Icterus from other fodders.
This affection has been noticed especially in sheep, but also in the
goat, horse, ox and stag as the result of eating lupins. The dog has
contracted the disease under experiment. It has been studied especially
in Northern Germany where the lupin is largely cultivated as a fodder
crop. The yellow lupin (Lupinus Luteus) is mainly to blame for the
disease, but the Lupinus Albus and Augustifolius are also spoken of as
factors.
The disease caused by altered seeds and straw of the lupin is mainly
characterized by jaundice, fatty degeneration of the hepatic cells and
hypertrophy of the connective tissue of the liver causing acute atrophy
of the organ.
_Causes._ The essential cause of the disease appears to be the
consumption of lupins. But all lupins are not equally poisonous. Those
taken from one portion of a field are harmless, while those from another
are toxic. In stacks built in the field and weathered the upper and
outer portions are often harmless while the interior remains poisonous.
It would seem as if the poison were washed off by the rain, or deprived
of its potency by the action of the air. It successfully resists dry
heat, for three hours at boiling temperature, but is rendered harmless
by steam acting under the pressure of two atmospheres for the same
length of time. A poisonous principle (lupino-toxine) has been obtained
from the toxic lupins but it is not quite certain that this is the sole
toxic ingredient. This agent is extracted from the powdered seeds by
macerating them for two hours in a soda solution (in which it is very
soluble) at 102° F., and purified by treating the solution successively
with acetic acid, lead acetate, hyposulphuric acid and alcohol. This
agent produces the symptoms of lupinosis in the acute or chronic form
according to the doses of the agent administered. Eichhorn and
Baumstarch have isolated from lupins an alkaloid analogous to
_conicine_: Stener found an alkaloid which he believed to be
_methylconicine_: Baumert attributed the activity to another alkaloid
_lupinine_. It is not definitely known whether the poisoning is usually
effected by a simple poison or by a combination of several. Nor is it
certain whether the toxic matter is a normal product of lupins grown on
particular soils and under given conditions and harvested at a
particular stage of growth, or if it is the product of a cryptogamic or
bacterial growth. Some leguminous seeds are poisonous at a given stage
of ripening but there is as yet no proof of lupinosis being confined to
any particular stage. The common moulds often grow on lupins without
rendering them poisonous, but it does not follow that some less familiar
cryptogam is equally harmless under all circumstances. The soda extract
of the poisonous lupins was deadly though it contained no cryptogams,
but it is not shown that it was free from soluble chemical products
(toxins) of the cryptogams. The same remark applies with equal force to
the bacteria which have been invoked as the cause of the poisons. Though
not themselves present in a given deadly extract of the lupins this does
not exclude from such extract the toxic products of bacterial growth. It
is claimed that Arnold has produced lupinosis with lupins that had been
first robbed of their alkaloids. But the absence of alkaloids does not
prove the absence of nonbasic (neutral) poisons, of vegetable,
cryptogamic or bacterial origin.
That certain lupins contain a deadly poison is certified, but the
precise source of the poison remains to be demonstrated.
In estimating causes we must take into account the lessened power of
resistance of animals lacking in constitutional strength and vigor. Thus
sheep suffer far more severely than horses, oxen, or even goats. Ewes
and lambs perish in greater numbers than rams, hoggets and wethers.
_Symptoms in Sheep._ In the acute form the disease appears suddenly, as
manifested by anorexia, hyperthermia, rapid and oppressed breathing,
accelerated pulse, stupor, vertigo, and not unfrequently swellings of
lips, ears or face. Inappetence may be first manifested by the rejection
of poisonous lupins, while sound ones and especially other food are
still eaten, but soon all are refused alike. Temperature, which may
reach 104° to 106° F. on the next day after feeding on the poison, may
rise and fall day by day, and finally fall materially as a herald of
death. Respiration rises to 100 per minute and becomes labored or
panting, with, in some cases, a bloody froth in the nostrils. The pulse
rising to 130 and upwards keeps pace with the hyperthermia and general
excitement. Vertigo is shown in the staggering gait when moved, and by a
tendency to steady by resting the head on the trough, rack, fence or
ground. The recumbent position is often preferred, the head being
extended on the ground, and the animal remaining oblivious to all
efforts to raise him—even to blows. Sometimes there is stupor, and at
others hyperæsthesia, or indications of fear. There is grinding of the
teeth, and sometimes trismus (Schütz, Kotelman).
In two or three days jaundice is shown, more especially in the
conjunctiva and the urine. The latter, however, is not unfrequently
colored with blood, and contains albumen, bile acids, and renal
epithelium and casts. It is passed frequently in small quantity, so that
its condition is easily ascertained.
The fæces are at first scanty and hard with a coating of yellowish
mucus, and it may be streaks of blood. Later they are uniformly stained
of a dark brown, and diarrhœa may alternate with the constipation.
Emaciation advances with rapid strides.
Death may occur as early as one day after the attack but is usually
deferred to the fourth or fifth.
A steady amelioration of all the symptoms may be welcomed as a precursor
of recovery.
In the _chronic form_ jaundice may be entirely absent, and a subacute
gastro-enteritis may be attended by emaciation and anæmia. Roloff has
frequently found the implication of the other mucosæ especially those of
the nose and eyes which become catarrhal, and Zurn notes the implication
of the skin of the face with exudations, swellings and the formation of
sores and scabs on the eyelids, lips, ears, etc.
_Lesions in Sheep._ The prominent lesions are parenchymatous
inflammation of the liver and kidneys, muco-enteritis, enlargement of
the spleen, and icterus, with more or less blood extravasation.
The liver is the seat of acute hepatitis. It is usually swollen and
abnormally friable, with a yellowish color often as deep as citron. The
parts recently attacked exhibit albuminoid infiltration and cloudy
swelling, the older lesions show fatty or granular degeneration. These
changes exist especially in the hepatic cells, and fatty metamorphosis
bears a direct relation to the obesity of the sheep. If the patient has
survived the first few days, the liquefied products are absorbed, there
is a relative increase of the interstitial connective tissue and the
volume of the organ is materially decreased (acute yellow atrophy of the
liver, Schütz). In chronic cases, the hypertrophy of the interstitial
connective tissue is the most prominent feature, constituting a distinct
cirrhoses (fibroid induration) and the atrophy becomes very pronounced
while the surface is very irregular and uneven. The gall bladder is
distended, and its mucosa congested.
Jaundice, which may be little marked apart from the conjunctiva, is
usually shown in the subcutaneous connective tissue, the skin of the
abdomen, the omentum and mesentery, but according to Cadeac is never
shown in cartilage, bone nor tendon.
The kidneys show parenchymatous inflammation, congestion, swelling which
gives a hardness of touch through the resisting fibrous envelope, and
often a pervading shade of yellow. The epithelium of the uriniferous
tubes is cloudy, turbid and granular and the tubes themselves contain
cylindroid casts. The bladder is catarrhal and has been too irritable to
contain urine.
The spleen is tumid, soft, reddish gray, and on section shows excess of
blood, pulp, and here and there marbling by fibrinous exudate.
The heart is pale, granular, friable, with a tinge of yellow and with a
slight citron colored effusion in the pericardium. The cardiac blood is
dark and thick but coagulates and brightens in color on exposure to the
air.
There is usually some œdema of the lung, larnyx and pia mater.
There are catarrhal lesions of the abomasum and entire intestinal canal
with granular degeneration of the epithelium and spots and patches of
arborescent congestion and hæmorrhage. The icteric tint is usually
distinct.
_Prognosis_ is always grave. Acute cases are almost always fatal.
Chronic cases due to eating lupins in which the poison is relatively
weak, or a very restricted amount of the more poisonous lupins, may
recover. This mortality is very serious in the affected districts 5.8
per cent. of all the sheep of some districts in Pommerania perishing
yearly from this affection and entailing the loss of almost the same
number of lambs (Von Below-Seleske).
_Prevention._ Radical prevention can be secured by the exclusion of
lupins from the ration. Where this is undesirable the fields that
produce poisonous lupins can be ascertained and devoted to the
production of other crops. When a crop of lupins has already been
produced on a dangerous field the poison may be extracted from the
fodder or subjected to the action of an antidote. Fortunately the poison
is concentrated on the surface of the lupin and is easily washed off.
Dammann advises to leave the cut forage exposed to the rain so that the
poison may be washed off. A more prompt and effective plan would be to
put the fodder under a stream of water from a hose, and it could be fed
while still fresh and unaltered. Friedberger and Fröhner directs that
the forage be steeped for forty-eight hours in a soda solution (1:100)
to dissolve off the offensive matter, after which it may be washed and
safely fed.
Glaser would put the lupins in a silo, in alternate layers with some
material which rapidly undergoes acid fermentation (brewers grains,
maize, pulped roots). The acid renders the poison insoluble and is
directly antidotal. To develop this acid it is important to put the
materials into the silo before they have become too far matured.
The destruction of the poison by steaming the fodder under a pressure of
two atmospheres, as recommended by Kuhn and Roloff requires a too
elaborate apparatus for ordinary use.
_Therapeutic treatment._ The first desideratum is to render insoluble
any poison which has already entered the alimentary canal. Alkalies, as
solvents and distributers of the poison must be carefully avoided and
acids (acetic, nitric, hydrochloric, sulphuric) freely used. These may
be mixed with the drinking water or given from a bottle. If appetite is
still retained, they may be mixed with the food, or acid aliment (sour
ensilage, old grains, or fermented swill) may be supplied.
The next resort is a purgative to eliminate the poison from the
alimentary canal. But the cathartics usually given to the ruminants are
dangerous. Sulphate of soda undergoing decomposition, furnishes an
alkaline solvent for the poison. Castor oil is therefore to be
preferred.
An abundance of water will favor the action of both bowels and kidneys
and hasten the elimination of the poison which may have been already
absorbed into the system.
European writers recommend the use of the flesh as human food, unless
the animal had reached the last stage of the disease.
_Symptoms of Lupinosis in the Horse._ There is always the history of the
presence of lupins in the oats, or of lupin straw as a food or litter.
Though less fatal than in sheep the disease sets in with great severity,
the symptoms referring especially to gastro-enteritis, and disorders of
innervation. There is complete anorexia, impaired sensibility, dullness
and stupor, the head resting on the manger or drooping with the nose
near the ground. There is grinding of the teeth, colicy symptoms, and
constipation, the fæces being passed as a few small, hard balls covered
with mucus and fœtid. Urine is passed frequently in small amount and
albuminous. There is more or less hyperthermia (rising at times to 102°
to 103°), the respiration is hurried (36 to 40 per minute) and pulse is
rapid (60 per minute). Jaundice is usually present but less prominent
than in sheep. When moved the animal sways unsteadily or staggers.
Butzert notices, in addition to the above, a thick orange colored
discharge from the nose, and the formation of sores and scabs
(mummification) of the lingual mucous membrane, of the lips, of the
skin, of the face, and of the pastern, and swelling of the lower parts
of the limbs.
_Diagnosis._ The development of disease with the above symptoms, in the
inmates of a single stable, or in horses having a common ration, in
which the lupines are found, will make diagnosis easy and reasonably
certain.
_Prognosis_ is hopeful or confident. The disease is not fatal in the
horse.
_Treatment_ should follow the same lines as in sheep.
_Allied or identical diseases._ Friedberger and Fröhner quote a number
of outbreaks of hepatic inflammation or disorder with icterus in the
absence of lupins, but on rations that were otherwise faulty. Haubner
describes a “malignant icterus” in sheep fed on malted potatoes; Sander
records a “hepatic typhus” in the horse when fed on inundated pastures;
Reinemann and Jansen speak of a similar affection in animals fed on the
straw of peas, beans and vetches.